Sodium currents in vagotomized primary afferent neurones of the rat.

1. Nodose ganglion neurones (NGNs) become less excitable following section of the vagus nerve. To determine the role of sodium currents (I(Na)) in these changes, standard patch-clamp recording techniques were used to measure I(Na) in rat NGNs maintained in vivo for 5-6 days following vagotomy, and then in vitro for 2-9 h. 2. Total I(Na) and I(Na) density in vagotomized NGNs were similar to control values. However, steady-state I(Na) inactivation in vagotomized NGNs was shifted -9 mV relative to control values (V(1/2), -74 +/- 2 vs. -65 +/- 2 mV, P < 0.01) and I(Na) activation was shifted by -7 mV (V(1/2), -21 +/- 2 vs. -14 +/- 2 mV, P < 0.006). I(Na) recovery from inactivation was also slower in vagotomized NGNs (fast time constant, 2.8 +/- 0.4 vs. 1.6 +/- 0.3 ms, P < 0.02). 3. The fraction of I(Na) resistant to 1 microM tetrodotoxin (TTX-R) was halved in vagotomized NGNs (21 +/- 8 vs. 56 +/- 8 % of total I(Na), P < 0.05). This change from TTX-R I(Na) to TTX-sensitive (TTX-S) I(Na) may explain altered I(Na) activation, inactivation and repriming in vagotomized NGNs. 4. The contribution of alterations in I(Na) to NGN firing patterns was assessed by measuring I(Na) evoked by a series of action potential (AP) waveforms. In general, control NGNs produced large, repetitive TTX-R I(Na) while vagotomized NGNs produced smaller TTX-S I(Na) that rapidly inactivated during AP discharge. We conclude that TTX-R I(Na) is important for sustained AP discharge in NGNs, and that its diminution underlies the decreased AP discharge of vagotomized NGNs.